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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Anapc2tm2Kna
targeted mutation 2, Kim Nasmyth
MGI:3029826
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Anapc2tm2Kna/Anapc2tm2Kna involves: 129P2/OlaHsd * C57BL/6 MGI:3686617
cn2
Anapc2tm1Kna/Anapc2tm2Kna
Tg(Mx1-cre)1Cgn/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3686618


Genotype
MGI:3686617
hm1
Allelic
Composition
Anapc2tm2Kna/Anapc2tm2Kna
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Anapc2tm2Kna mutation (0 available); any Anapc2 mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die before E6.5 as no homozygous embryos are found at E6.5 or E9.5




Genotype
MGI:3686618
cn2
Allelic
Composition
Anapc2tm1Kna/Anapc2tm2Kna
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Anapc2tm1Kna mutation (0 available); any Anapc2 mutation (36 available)
Anapc2tm2Kna mutation (0 available); any Anapc2 mutation (36 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most die during the second week after the first pI/C injection to induce cre-mediated deletion of Anapc2 in the liver and lymphocytes

liver/biliary system
• hepatocytes of mutants treated with pI/C lack glycogen
• hepatocytes are greatly enlarged, lack nuclear membranes, and contain condensed chromosomes in 6 of 10 mutants after pI/C injection
• 72% of mitotic hepatocytes are in a prometaphase-like state with condensed chromatin
• levels of the liver enzymes alanine aminotransferase and glutamate dehydrogenase are highly elevated in pI/C injected mutants, indicating functional impairment and damage of hepatocytes
• quiescent hepatocytes of some but not all livers enter into a proliferative state, resulting in a mitotic arrest
• 2/3 hepatectomy in mutants transplanted with wild-type bone marrow and treated with pI/C caused 70% of hepatoctyes to re-enter the cell cycle and embark on proliferation and arrest in metaphase 3 to 5 days after hepatectomy
• die from acute liver failure after pI/C injection

hematopoietic system
• the 4 of 10 mutants injected with pI/C with normal livers and 2 of 6 with abnormal livers show severe anemia
• the 4 of 10 mutants injected with pI/C with normal livers show decreased hemoglobin levels

homeostasis/metabolism
• levels of bilirubin are highly elevated in pI/C injected mutants
• levels of the liver enzymes alanine aminotransferase and glutamate dehydrogenase are highly elevated in pI/C injected mutants, indicating functional impairment and damage of hepatocytes
• hepatocytes of mutants treated with pI/C lack glycogen

skeleton
• develop severe bone marrow aplasia within 4 days of pI/C injection; by day 4, majority of nucleated cells disappear from the bone marrow which contains mainly erythrocytes and a few lymphocytes

cellular
• quiescent hepatocytes of some but not all livers enter into a proliferative state, resulting in a mitotic arrest
• 2/3 hepatectomy in mutants transplanted with wild-type bone marrow and treated with pI/C caused 70% of hepatoctyes to re-enter the cell cycle and embark on proliferation and arrest in metaphase 3 to 5 days after hepatectomy





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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory